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The Nrf2-Keap1 pathway: A secret weapon against pesticide persecution in Drosophila Kc cells

文献类型： 外文期刊

作者： Chen, Lu 1 ; Zhang, Tingting 1 ; Ge, Mengying 1 ; Liu, Yahui 1 ; Xing, Yuping 1 ; Liu, Liu 1 ; Li, Fengliang 2 ; Cheng, L 1 ;

作者机构： 1.Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Biodivers & Biotechnol, Nanjing 210023, Peoples R China

2.Guizhou Acad Agr Sci, Inst Plant Protect, Guiyang 550009, Peoples R China

关键词： Nrf2; Oxidative stress; Apoptosis; Resistance

期刊名称：PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY （ 影响因子：3.963； 五年影响因子：4.454 ）

ISSN： 0048-3575

年卷期： 2020 年 164 卷

页码：

收录情况： SCI

摘要： Nrf2-Keap1 pathway defends organisms against the detrimental effects of oxidative stress, and play pivotal roles in preventing xenobiotic-related toxicity. We designed experiments to explore and verify its role and function under deltamethrin (DM) stress. In experiments, DM was selected as the inducer, and Drosophila Kc cells were treated as the objects. The result showed the oxidative stress of cells proliferated in a very short time after DM treatment, reaching the maximum after one hour of treatment. The experimental data showed Nrf2 could be upregulated and activated by DM which were manifested by the increase of Nrf2 mRNA, Nrf2 protein in the nucleus and the expression of detoxification enzyme genes. We further tested the activity of all groups, and found the survival rate of cells was basically proportional to the expression of Nrf2. Based on the above experimental results, Keap1 overexpression (K+), Nrf2 overexpression (N+) or interference (N-) cells were used to verified the relationship between Nrf2, cell survival and detoxification enzymes expression. We found the cell survival rate of N+ group was significantly higher than that of other groups and the expression of detoxification enzymes were increased compared to the control group. These results demonstrated that Nrf2 is related to cell detoxification and associated with the tolerance to DM. Our evidence suggested Nrf2 is a potential therapeutic target for oxidative stress and a potential molecular target gene of resistance control.

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